Universidade Federal do Ceará Rua Tiburcio Cavalcante 2100/1201 CEP 60125-101 Fortaleza CE Brazil.
Mediators Inflamm. 1996;5(2):104-9. doi: 10.1155/S0962935196000178.
We investigated the participation of lipid mediators in an experimental immune complex (IC) arthritis model in rats. The animals were subjected to intraarticular injection of anti-bovine sertLm albumin (BSA) IgG antibodies followed by i.v. injection of BSA. Histopathological analysis of the synovial membranes disclosed infiltration of polymorphonuclear (PMN) cells and vascular congestion. Slight increase in vascular permeability, measured by Evans blue dye extravasation into the joints, was detected after 3 h of arthritis. Cellular influx into the articular cavities was most evident at the sixth hour of arthritis with predominance of PMN. Pretreatment with either indomethacin, a cyclooxygenase inhibitor, or L-660,711, a peptido-leukotriene antagonist, did not inhibit cell infiltration, whereas pretreatment with either L-663,536, a 5-lipoxygenase inhibitor, or L-655,240, a thromboxane antagonist, significantly inhibited the phenomenon. Pretreatment with WEB 2170, a platelet activating factor (PAF) antagonist, also significantly inhibited cell influx. These results suggest that thromboxane, LTB(4) and PAF mediate cell infiltration in this IC arthritis model.
我们研究了在大鼠实验性免疫复合物(IC)关节炎模型中脂质介质的参与。动物接受抗牛血清白蛋白(BSA)IgG 抗体的关节内注射,然后静脉注射 BSA。滑膜膜的组织病理学分析显示多形核(PMN)细胞浸润和血管充血。关节炎 3 小时后,通过 Evans 蓝染料渗出到关节中检测到血管通透性的轻微增加。关节炎第六小时关节腔内细胞浸润最为明显,PMN 占优势。用环氧化酶抑制剂吲哚美辛或肽类白三烯拮抗剂 L-660,711 预处理不能抑制细胞浸润,而用 5-脂氧合酶抑制剂 L-663,536 或血栓烷拮抗剂 L-655,240 预处理则显著抑制该现象。血小板激活因子(PAF)拮抗剂 WEB 2170 的预处理也显著抑制细胞浸润。这些结果表明,血栓烷、LTB4 和 PAF 介导了这种 IC 关节炎模型中的细胞浸润。